Clostridia are ubiquitous in the soil and in the normal microbial flora of humans and animals. These infections are diagnosed by recognition of a characteristic lesion coupled with tissue Gram stains and bacterial culture. Wound infections are controlled by administration of antimicrobial agents e.
Tetanus is characterized by twitching of muscles around a wound, pain in neck and jaw muscles trismus , and around the wound. Patients have no fever, but sweat profusely and exhibit muscle rigidity and spasms. The infection is initiated as a result of contamination of a wound with C tetani. The anaerobic tissue environment facilitates C tetani replication and secretion of exotoxins.
A spasmogenic toxin, tetanospasmin, fixes to inhibitory neurons and blocks the release of neurotransmitters, glycine and gamma-aminobutyric acid. Host defenses are essentially absent. There is little, if any, inate immunity and the disease does not produce immunity in the patient. Active immunity follows vaccination with tetanus toxoid.
C tetani is found worldwide. Ubiquitous in soil, it is occasionally found in intestinal flora of humans and animals. Diagnosis is primarily by the clinical symptoms above. The wound may not be obvious. Furthermore, C tetani is recovered from only one-third of all implicated wounds. The administration of tetanus toxoid is a preventive measure.
C tetani infection is treated with antimicrobial agents metronidazole or penicillin and by local wound debridement. Other measures include tetanus immunoglobulin and supportive therapy.
These infections may have early gastrointestinal symptoms. The cranial nerves are initially affected, followed by descending, symmetric paralysis of motor nerves, with critical involvement of the respiratory tree. Muscle paralysis may occur. C botulinum consists of several biochemically distinct groups of organisms that produce botulinum toxin.
There are three forms: 1 adult botulism, caused by ingestion of preformed toxin in food; 2 infant botulism, in which the organism replicates and secretes toxin in the intestinal tract; and 3 wound botulism, in which the organism replicates in the wound and secretes toxin.
Toxin binds to neuromuscular junctions of parasympathetic nerves and interferes with acetylcholine release, causing flaccid muscle paralysis. C botulinum is distributed worldwide, and is ubiquitous in soil. Improper heating of canned foods is a major factor in botulism food poisoning.
Diagnosis is from the clinical symptoms above , especially gastrointestinal and neurological symptoms, coupled with laboratory confirmation. A finding of normal spinal fluid helps to eliminate the possible diagnosis of numerous other central nervous system disorders.
The best means of control is to eliminate the toxin source via proper food handling. Once the food poisoning is diagnosed, treatment measures should include an attempt to neutralize unbound toxin. Supportive care is of primary importance. Patients can present with a spectrum of disease that varies from uncomplicated antibiotic-associated diarrhea to antibiotic-associated pseudomembranous colitis that may be fatal. C difficile is the only species.
There are no defined serotypes. Toxigenic and nontoxigenic strains exist. The former produce varying amounts of toxin A enterotoxin and toxin B cytotoxin. Broad spectrum antibiotic therapy eliminates much competing normal flora, permitting intestinal overgrowth of toxigenic C difficile. C difficile is a component of the normal intestinal flora of a small percentage of healthy adults and of a relatively large percentage of healthy neonates.
It also may be found in the environment, especially in hospitals. Metronidazole and vancomycin should be used therapeutically. However, relapses can occur. Supportive therapy may be needed. Clostridium perfringens causes food poisoning and necrotizing enteritis.
C sordellii causes bacteremia, endometritis and nonbacteremic infections. C septicum is correlated with the presence of cancer. C tertium is associated with bacteremia. Of the anaerobes that infect humans, the clostridia are the most widely studied. They are involved in a variety of human diseases, the most important of which are gas gangrene, tetanus, botulism, pseudomembranous colitis and food poisoning.
In most cases, clostridia are opportunistic pathogens; that is, one or more species establishes a nidus of infection in a particular site in a compromised host. All pathogenic clostridial species produce protein exotoxins such as botulinum and tetanus toxins that play an important role in pathogenesis. Most generalizations about Clostridium have exceptions.
The clostridia are classically anaerobic rods, but some species can become aerotolerant on subculture; a few species C carnis, C histolyticum, and C tertium can grow under aerobic conditions. Most species are Gram-positive, but a few are Gram-negative. Also, many Gram-positive species easily lose the Gram reaction, resulting in Gram-negative cultures.
The clostridia form characteristic spores, the position of which is useful in species identification; however, some species do not sporulate unless exposed to exacting cultural conditions. Many clostridia are transient or permanent members of the normal flora of the human skin and the gastrointestinal tracts of humans and animals. Unlike typical members of the human bacterial flora, most clostridia can also be found worldwide in the soil.
Because clostridia are ubiquitous saprophytes, many isolated from clinical specimens are accidental contaminants and not involved in a disease process. Because these organisms are normally found on the skin, even a pure culture of clostridia isolated from blood may have no clinical significance. In determining the importance of a clinical isolate of clostridia, the clinician should consider the frequency of isolation of the species, the presence of other microbes of pathogenic potential, and the clinical symptoms of the patient.
Many clostridial infections can be controlled by antibiotic therapy e. Antitoxin therapy and toxoid immunization are clearly useful in some clostridial infections, such as tetanus. Clostridial wound infections may be divided into three categories: gas gangrene or clostridial myonecrosis, anaerobic cellulitis, and superficial contamination.
Gas gangrene can have a rapidly fatal outcome and requires prompt, often severe, treatment. The more common clostridial wound infections are much less acute and require much less radical treatment; however, they may share some characteristics with gas gangrene and must be included in the differential diagnosis. Gas gangrene is an acute disease with a poor prognosis and often fatal outcome Fig. Initial trauma to host tissue damages muscle and impairs blood supply. This lack of oxygenation causes the oxidation-reduction potential to decrease and allows the growth of anaerobic clostridia.
Initial symptoms are generalized fever and pain in the infected tissue. As the clostridia multiply, various exotoxins including hemolysins, collagenases, proteases, and lipases are liberated into the surrounding tissue, causing more local tissue necrosis and systemic toxemia. Infected muscle is discolored purple mottling and edematous and produces a foul-smelling exudate; gas bubbles form from the products of anaerobic fermentation.
As capillary permeability increases, the accumulation of fluid increases, and venous return eventually is curtailed. As more tissue becomes involved, the clostridia multiply within the increasing area of dead tissue, releasing more toxins into the local tissue and the systemic circulation.
Because ischemia plays a significant role in the pathogenesis of gas gangrene, the muscle groups most frequently involved are those in the extremities served by one or two major blood vessels. Pathogenesis of gas gangrene caused by C perfringens. Clostridial septicemia, although rare, may occur in the late stages of the disease. Severe shock with massive hemolysis and renal failure is usually the ultimate cause of death. The incubation period, from the time of wounding until the establishing of gas gangrene, varies with the infecting clostridial species from 1 to 6 days, but it may be as long as 6 weeks.
Average incubation times for the three most prevalent infecting organisms are as follows: C perfringens , 10—48 hours; C septicum , 2—3 days; and C novyi , 5—6 days. Because the organisms need time to establish a nidus of infection, the time lag between wounding and the appropriate medical treatment is a significant factor in the initiation of gas gangrene. Like gas gangrene, clostridial cellulitis is an infection of muscle tissue, but here the infecting organisms invade only tissue that is already dead; the infection does not spread to healthy, undamaged tissue.
Clostridial cellulitis has a more gradual onset than gas gangrene and does not include the systemic toxemia associated with gas gangrene. Pain is minimal, and although only dead tissue is infected, the disease can spread along the planes between muscle groups, causing the surrounding tissue to appear more affected than it actually is. Anaerobic cellulitis may cause formation of many gas bubbles, producing infected tissue that looks similar to the gaseous tissue of gas gangrene.
Some tissue necrosis does occur, but it is caused by decreased blood supply and not invasion by the infecting organism. With adequate treatment, anaerobic cellulitis has a good prognosis.
Superficial contamination, the least serious of the clostridial wound infections, involves infection of only necrotic tissue. Usually, the patient experiences little pain, and the process of wound healing proceeds normally; however, occasionally an exudate may form and the infection may interfere with wound healing.
Superficial wound contamination caused by clostridia usually involves C perfringens , with staphylococci or streptococci, or both, as frequent co-isolates. Clostridial wound infections usually are polymicrobic because the source of wound contamination feces, soil is polymicrobic.
Other bacterial isolates may be any of a wide number and variety of organisms for example, Proteus, Bacillus, Escherichia, Bacteroides, Staphylococcus. The distinctive or unique properties of the causative agents of gas gangrene are difficult to list; morphologic characteristics and biochemical reactions vary among these species, and a reliable laboratory manual should be consulted for their proper identification.
Isolation of 10 7 or more clostridia per milliliter of wound exudate is strong evidence for a clostridial wound infection. Each of these types produces a semi-unique spectrum of protein toxins. Alpha-toxin a lecithinase, also called phospholipase-C and theta-toxin oxygen-labile cytolysin are both considered important in the disease pathology. Alpha-toxin is lethal and necrotizing; it lyses cell membrane lecithins, disrupting cell membranes and causing cell death.
Theta-toxin also contributes to rapid tissue destruction by several mechanisms. At the site of infection, theta-toxin acts as a cytolysin, promoting direct vascular injury; lower toxin concentrations activate polymorphonuclear leukocytes and endothelial cells, promoting distal vascular injury by stimulating leukocyte adherence to the endothelium.
The result is leukostasis, thrombosis, decreased perfusion, and tissue hypoxia. Theta-toxin also mediates the production of shock through induction of inflammatory mediators such as platelet activating factor, tumor necrosis factor, interleukin 1 and interleukin 6. All clostridial wound infections occur in an anaerobic tissue environment caused by an impaired blood supply secondary to trauma, surgery, foreign bodies, or malignancy.
Contamination of the wound by clostridia from the external environment or from the host's normal flora produces the infection. The detailed pathogenesis of the disease is intimately associated with the clinical presentation as described above Fig. Host defenses against gas gangrene and other clostridial wound infections are mostly ineffective.
Even repeated episodes of clostridial wound infection do not seem to produce effective immunity. Clostridial spores are ubiquitous in the soil, on human skin, and in the gastrointestinal tracts of humans and animals. Thus, the causative agents of clostridial wound infections are not environmentally restricted.
Even operating theaters can be habitats for infecting clostridial organisms and spores. The incidence of clostridial wound infections has declined with the advance of prompt, adequate medical treatment. Historically, war casualties have had the greatest incidence of gas gangrene; however, the prompt evacuation and medical attention given United States casualties in the Vietnam war greatly decreased the incidence of gas gangrene in these soldiers, emphasizing the importance of prompt medical treatment.
Diagnosis of clostridial wound infections is based on clinical symptoms coupled with Gram stains and bacterial culture of clinical specimens. Gas gangrene, once initiated, may spread and cause death within hours.
By the time the typical lesions of gas gangrene are evident, the disease usually is firmly established and the physician must treat the patient on a clinical basis without waiting for laboratory confirmation. Characteristic lesions and the presence of large numbers of Gram-positive bacilli with or without spores in a wound exudate provide strong presumptive evidence.
In contrast to tissue infections caused by Staphylococcus aureus , there is typically an absence of polymorphonuclear leukocytes at the site of infection, likely due to the presence of clostridial toxins. Spores are rare in cultures of C perfringens , the most common etiologic agent of these diseases. A commonly used laboratory test for presumptive identification of C perfringens is the Nagler reaction which detects the presence of alpha-toxin phospholipase-C , one of the most prominent toxins produced by C perfringens.
However, several other species of clostridia also have a positive Nagler reaction, and thus this test is not entirely specific for C perfringens. Discussion of the differential diagnosis of clostridial wound infections appropriately includes streptococcal myositis, as this disease can be characterized by an edematous, necrotizing, often gaseous lesion.
Like anaerobic cellulitis and superficial contamination with clostridia, streptococcal myositis is a relatively localized disease, but its later stages may include some systemic toxicity that mimics the toxemia of gas gangrene. Correction of the anaerobic conditions combined with antibiotic treatment form the basis for therapy.
Penicillin is the drug of choice for all clostridial wound infections; chloramphenicol is a second-choice antibiotic. Successful treatment of the less severe forms of clostridial wound infections includes local debridement and antibiotic therapy; after these measures are taken, patient recovery usually proceeds along a steady, positive course.
Treatment of gas gangrene includes radical surgical debridement coupled with high doses of antibiotics. Blood transfusions and supportive therapy for shock and renal failure also may be indicated.
The usefulness of gas gangrene antitoxin is currently a disputed matter. Some physicians maintain that the efficacy of this polyvalent antitoxin has been proved in the past, but better medical care now may have eliminated the need for its use. Others believe that because of insufficient data, antitoxin should be administered systemically as early as possible after diagnosis, and that the antitoxin should be injected locally into tissue that cannot be excised. Obviously, prevention of wound contamination is the single most important factor in controlling clostridial wound infections.
In the past, immunization has been considered a possible preventive measure for gas gangrene; however, several factors have discouraged the use of active immunization, including difficulty in preparing a suitable antigenic toxoid, availability of prompt wound treatment, and accessibility of effective therapeutic agents.
Tetanus is a severe disease caused by the toxin of C tetani Fig. This organism grows in a wound and secretes a toxin that invades systemically and causes muscle spasms. The initial symptom is cramping and twitching of muscles around a wound. The patient usually has no fever but sweats profusely and begins to experience pain, especially in the area of the wound and around the neck and jaw muscles trismus.
Portions of the body may become extremely rigid, and opisthotonos a spasm in which the head and heels are bent backward and the body bowed forward is common. Complications include fractures, bowel impaction, intramuscular hematoma, muscle ruptures, and pulmonary, renal, and cardiac problems.
C tetani is an anaerobic gram-positive rod that forms terminal spores, giving it a characteristic tennis racquet appearance. Some strains do not sporulate readily, and spores may not appear until the third or fourth day of culture. Most strains are motile with peritrichous flagella; colonies often swarm on agar plates, but some strains are nonflagellated and nonmotile.
The presence of C tetani should be suspected on isolation of a swarming rod that produces indole and has terminal spherical spores, but does not produce acid from glucose. Toxigenic C tetani contains a plasmid that produces a toxin called tetanospasmin, but nontoxigenic strains also exist.
Tetanospasmin is responsible for the infamous toxemia called tetanus. The two animal species most susceptible to this toxemia are horses and humans. As with all clostridial wound infections, the initial event in tetanus is trauma to host tissue, followed by accidental contamination of the wound with C tetani Fig.
Tissue damage is needed to lower the oxidation-reduction potential and provide an environment suitable for anaerobic growth. Once growth is initiated, the organism itself is not invasive and remains confined to the necrotic tissue, where the vegetative cells of C tetani elaborate the lethal toxin. The incubation period from the time of wounding to the appearance of symptoms varies from a few days to several weeks, depending on the infectious dose and the site of the wound the more peripheral the wound, the longer the incubation time.
Munro introduced himself and told Belva that he thought he knew her. Munro would end up dating someone else until March, but after that relationship ended Belva and Munro began talking on the phone. And talk for 30 or 40 minutes. But he never asked me out. Finally, Munro did ask her out. He asked her to join him at a Fourth of July picnic party.
An absolute hunk. The two won a Fourth of July costume contest at the picnic. From there Belva recalls things moving quickly. She said she knew by September that if things kept progressing, they would get married.
Belva wanted a sign that she was supposed to marry Munro. Whether it was finding the perfect wedding dress by accident or being able to book the best wedding photographer in Charlotte, Belva got multiple signs.
I just knew that it was what I was supposed to do. When marrying Belva, Munro became a stepdad to her two teenage daughters. He loved them like they were his. Belva says that Munro was the role model her daughters needed. He was very loving to them and if they called, he would want me to put them on speakerphone so he could hear every word. He urged her to pursue art. He always seemed to love me more. Neurotoxins are produced by two Clostridium species namely, Clostridium tetani tetanus toxin and Clostridium botulinum botulinum toxin.
The two toxins share several features including heavy H and light L chains that are bound by a disulfide bond. Produced by C. In doing so, the toxin blocks the release of neurotransmitter acetylcholine thus affecting muscle contraction. Within the nervous system, the neurotransmitter is the primary neurotransmitter that sends signals to cells thus contributing to the contraction of the smooth muscle as well as the dilation of blood vessels.
By blocking the release of this neurotransmitter, muscle contraction is affected, which results in muscle weakness and paralysis. Tetanus toxin is released by Clostridium tetani and is the primary cause of tetanus. Typically, spores of the bacteria C. Once in the body, the spore starts to germinate followed by the release of toxins into the bloodstream as well as the lymphatic system.
From the bloodstream and lymphatic systems, the toxin is taken up through lower motor neurons and transported to the spinal cord or the brainstem. Although the toxin affects the central nervous system on several points, it significantly affects the neurotransmitter by blocking its release at the central inhibitory interneurons.
In turn, this results in the disinhibition of the lower motor neurons which leads to uncontrollable contraction of muscles. Some of the symptoms of tetanus Tetanus toxin include:. Enterotoxin, a toxin released by C. In the body in vivo the toxin is released during bacterial sporulation. The toxin is released into the intestinal lumen where it binds to the claudin receptors.
This results in the formation of pre-pores and consequently functional pores CH-1 pore that cause oncosis through calcium influx. Some of the other toxins released by Clostridium bacteria include:. Among Clostridium, a majority are Gram-positive rods. Although these bacteria may appear Gram-positive, they can lose this appearance under various conditions.
In cases of extended incubation, some of the Clostridium species have been shown to lose their Gram-positive appearance. A few species, however, have been shown to be Gram-negative and will stain pink during Gram staining. Today, well over species belonging to the genus Clostridium have been identified.
Of these, at least 30 are of clinical significance. To observe and identify the species, Gram staining technique can be used. Place the slide under the microscope and view under immersion oil - compound light microscope or phase-contrast microscope may be used to view the cells. When viewed under the microscope, one may observe the following, depending on the species:.
They may also be motile depending on the sample and sample preparation. Students will also notice that they are rod-shaped. They are also non-motile with no terminal poles. See also pages on heterotrophs , and more on unicellular organisms.
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